A complex network of cellular receptors, RNA targeting pathways, and small-molecule signaling provides robust plant immunity and tolerance to viruses. To maximize their fitness, viruses must evolve control mechanisms to balance host immune evasion and plant-damaging effects. The genus Potyvirus comprises plant viruses characterized by RNA genomes that encode large polyproteins led by the P1 protease. A P1 autoinhibitory domain controls polyprotein processing, the release of a downstream functional RNA-silencing suppressor, and viral replication. Here, we show that P1Pro, a plum pox virus clone that lacks the P1 autoinhibitory domain, triggers complex reprogramming of the host transcriptome and high levels of abscisic acid (ABA) accumulation. A meta-analysis highlighted ABA connections with host pathways known to control RNA stability, turnover, maturation, and translation. Transcriptomic changes triggered by P1Pro infection or ABA showed similarities in host RNA abundance and diversity. Genetic and hormone treatment assays showed that ABA promotes plant resistance to potyviral infection. Finally, quantitative mathematical modeling of viral replication in the presence of defense pathways supported self-control of polyprotein processing kinetics as a viral mechanism that attenuates the magnitude of the host antiviral response. Overall, our findings indicate that ABA is an active player in plant antiviral immunity, which is nonetheless evaded by a self-controlled RNA virus.

细胞受体、RNA 靶向途径和小分子信号传导的复杂网络提供了强大的植物免疫力和对病毒的耐受性。为了最大限度地提高其适应性，病毒必须进化出控制机制来平衡宿主免疫逃避和植物破坏作用。马铃薯Y病毒属包括以RNA基因组为特征的植物病毒，所述RNA基因组编码由P1蛋白酶领导的大多蛋白。 P1 自抑制结构域控制多蛋白加工、下游功能性 RNA 沉默抑制子的释放以及病毒复制。在这里，我们发现 P1Pro（一种缺乏 P1 自抑制结构域的李痘病毒克隆）会触发宿主转录组的复杂重编程和高水平的脱落酸 (ABA) 积累。一项荟萃分析强调了 ABA 与已知控制 RNA 稳定性、周转、成熟和翻译的宿主途径的联系。 P1Pro 感染或 ABA 引发的转录组变化在宿主 RNA 丰度和多样性方面表现出相似性。遗传和激素处理测定表明 ABA 促进植物对马铃薯病毒感染的抵抗力。最后，在存在防御途径的情况下，病毒复制的定量数学模型支持多蛋白加工动力学的自我控制，作为一种减弱宿主抗病毒反应强度的病毒机制。总体而言，我们的研究结果表明 ABA 在植物抗病毒免疫中发挥着积极作用，但自控 RNA 病毒却可以逃避这种免疫。